红景天苷对缺血再灌注大鼠脑损伤的保护作用

Protective effect and its mechanism of salidroside against cerebral ischemia-reperfusion injury

目的研究红景天苷对缺血再灌注大鼠脑组织损伤的保护作用。方法用线栓法制备大鼠大脑中动脉缺血再灌注(MCAO-I/R)模型,在缺血和再灌注即刻分别给予红景天苷5 mg·kg^(-1)进行保护。脑缺血1.5 h再灌注24 h后用Zea-Longa标准进行神经功能评分;TTC染色法测定大鼠脑梗死面积;用南京建成生物工程研究所的试剂盒检测大鼠脑组织内超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)的活性;用Western blot法测大鼠脑组织肿瘤坏死因子-α(TNF-α)的表达水平。结果红景天苷能缩小MCAO-I/R大鼠脑梗死面积(P<0.05),减轻脑神经功能损伤(P<0.05),提高脑内SOD的活性(P<0.05),降低MPO (P<0.01)和TNF-α水平(P<0.05)。结论红景天苷可以通过增加自由基的清除、降低白细胞浸润、减少炎症因子的表达,从而减轻缺血再灌注脑组织的损伤。

A/M To study the protective effect and the mechanism of salidroside against cerebral ischemia-reper-fusion injury in MCAO-I/R rats. METHODS Focal cerebral ischemia in rats was produced by 1.5 h occlusion of the middle cerebral artery （MCAO） and 24 h reperfusion. Salidroside （5 mg·kg^-1） was administered intravenously immediately after occlusion and reperfusion respectively. The neurologic deficit score was investigated according to Zea-Longa＇ s Standard. The infarct volume was assessed with software Image Pro 4.5 after TTC staining. The activities of superoxide dismutase（SOD） and myeloperoxidase （MPO） were estimated by test boxes produced by Nanjing Jiancheng Bioengineering Institute. The levels of tumor necrosis factor-alpha（TNF-α） in central neutral system were measured by western blot. RESULTS Compared with the model group, salidroside treatment can significantly decrease the neurologic deficit score （ P 〈 0.05）, reduce the moisture capacity（ P 〈 0.05） and the infarct volmne（ P 〈 0.05）. A significant increase in SOD activities was found in the salidroside treatment group, compared with the model control group （ P 〈 0.05）. Also, salidroside treatment decreased the levels of MPO activity（ P 〈 0.01 ） and inhibited the overexpression of TNF-α（ P 〈 0.05） in the brain. CONCLUSION Salidroside has a protective effect on cerebral ischemia-reperfusion injury and this effect is likely related to TNF-α.